L-Glutamine, and L-Carnitine

HIV infection and the progression to AIDS involves a long period of latent infection characterized by low levels of viral replication that slowly increase to the point of immunosup-pression.1 This progression is accelerated if the latent (non-reproducing) provirus in the nuclei of the lymphocyte is activated.2 Oxidative stress induces both viral activation of HIV and DNA damage, leading to immunosuppression.3-5 It is now generally accepted that a central pathologic feature of HIV disease involves oxidative stress, leading to programmed cell death (apoptosis) and depletion of CD4 cells.6,7 It has been hypothesized by Montagnier and others8,9 that the majority of T-helper (CD4+) cell loss (the cell most susceptible to fatal injury by HIV) actually occurs by apoptosis and not by direct HIV infection. This phenomenon has been seen in in vitro culture and in peripheral blood lymphocytes from HIV-infected patients.10 Evidence of increased oxidation reactions,11 depletion of the glutathione-based antioxi-dant defense system,12 and increased levels of oxygen radicals have been demonstrated in the blood and tissues of HIV-infected individuals.6 Elevated levels of hydroperoxides,13 malondialdehyde,14 and deficiencies of the critical antioxidant enzymes manganese superoxide dismutase, glutathione peroxidase, thioredoxin, and catalase have been demonstrated in plasma